Recently, Li et al.[51] reported that, in a xenograft mouse model of MM, scutellarin, a flavonoid glycoside and proteasome inhibitor, reduced disease progression and mitigated chemoresistance to bortezomib through multiple mechanistic pathways involving epigenetic regulation of c-MET/AKT/m-TOR by HDAC/miR-34a, as well as by NF-κB-mediated activation of the apoptotic cascade. The gene discussed is MET; the disease is Miyoshi myopathy.